The objective of this work is to study the molecular basis of teratomas that arise from germ cells. Working with the mouse as a model system we have found that the enzyme L-glycerol 3-phosphate dehydrogenase has one type of isozyme in the normal embryo and another type in the adult. Other investigators working with other embryonic or fetal isozymes have found that, in general, highly malignant tumors contain the embryonic or fetal isozyme forms. Based on these kinds of studies, they have hypothesized that this embryonic type of enzyme expression in tumors is irreversible. I have tested this hypothesis further by analyzing L-glycerol 3-phosphage dehydrogenase in several types of tumors of the mouse. In contrast to the results of other investigators with other isozyme systems, the expression of both adult and embryonic alpha-GPDH was observed and a necessary condition for embryonic isozyme expression was the physical form of the tumor. The embryonic isozyme was the major type only in the ascites tumors. All solid tumors expressed predominantly the adult isozyme. I am investigating further the nature of this kind of control mechanism by producing teratomas from strains of mice that possess the full range of alleles at the structural locus for L-glycerol 3-phosphate dehydrogenase. Once these tumors are produced, I intend to develop established cell lines from the tumors and study the mechanism for the transition from embryonic to adult isozyme expression in culture. The analyses will involve determining rates of enzyme synthesis and degradation with immunochemical techniques.